To our knowledge, this preliminary study is the first to examine OW/OB in pediatric BP specifically. A substantial proportion of subjects, 42%, were OW/OB. Lifetime history of physical abuse and SUD were each independently associated with a nearly three-fold increased prevalence of OW/OB. Younger age, non-Caucasian race, history of psychiatric hospitalization, and treatment with medications from ≥2 classes associated with weight gain were independently associated with OW/OB. Lifetime treatment with atypical antipsychotics was significantly associated with OW/OB in univariate but not regression analyses.
The prevalence of OW/OB among youth continues to increase, and recent national data indicate that approximately 34% of youth are OW/OB29
. The prevalence OW/OB among subjects in this study was approximately 15% greater than the national prevalence, and the prevalence of OB was approximately 20% greater29
. The difference in OW/OB approached significance (p=0.05). Similarly, recent epidemiologic data indicate that adults with BP have approximately 16% greater prevalence of OW/OB compared to those without BP7
. Therefore, although confirmatory controlled studies are needed to confirm this, present findings suggest that the association between BP and OW/OB may be of comparable magnitude among youth and adults.
Previous findings from adults with BP indicate that at least half and as many as two-thirds are OW/OB5,6,9,10
. Several classes of mood-stabilizing medications are associated with obesity among adults with BP5
, and with weight gain among youth with BP30
. Moreover, the impact of these medications on weight gain and other metabolic parameters may be greater among youth as compared to adults31
. Indeed, a recent study of hospitalized children and adolescents exposed to atypical antipsychotics, half of whom carried a diagnosis of BP, reported a 53% prevalence of OW32
. Present findings provide further support for these associations among youth with BP despite that limited details regarding medication exposure were available (as described below).
In addition to the impact of medications, however, other putative explanations for the high prevalence of OW/OB among adults with BP have previously been described, and these may apply to youth as well. Previous studies have implicated excessive carbohydrate consumption, low rate and intensity of exercise, substance misuse, and maladaptive efforts at self-modulation of mood by over-eating33-37
. There may be a medication-independent propensity toward binge-eating that is inherent in BP, and which may result in OW/OB38
. Shared genetic factors and neurotransmitter abnormalities may underlie both of these conditions35
. Clearly, more research is needed to parse medication-related from illness-related contribution to OW/OB, consumptive behavior, and exercise in BP. Another factor that may be contributory is a relative paucity of physician advice and counseling. A recent study of adults with BP, schizophrenia, or neither, found that BP subjects were the least likely to report discussing dietary intake or physical activity with their physician33
. Although it is not known whether this is also true of youth with BP, strategies for incorporating such discussions in the treatment of BP youth are clearly indicated.
The association of non-Caucasian race with greater prevalence of OW/OB in the present study is consistent with epidemiologic data28
. Age was significantly associated with OW/OB in multivariate, but not univariate, analyses. This could be because age is significantly associated with other variables such as SUD, medications, and psychiatric hospitalizations. Age accounted for a significant proportion of the variance in OW/OB once the contribution of the other variables was controlled for. The significant association of younger age with OW/OB suggests the possibility that children with BP may be particularly susceptible to OW/OB; however this finding requires replication. Kilbourne and colleagues also found that African-American race and younger age are each associated with lower likelihood of a physician discussing dietary intake and physical activity with adult patients with BP and schizophrenia33
. It is possible that these demographic variables also contribute to differences in weight-related counseling among youth with BP.
The finding of an association of obesity with physical abuse has been previously identified37
. A recent retrospective population-based study examined the association between multiple types of early adversity with weight and obesity. Physical abuse during childhood was the strongest predictor of obesity (BMI > 30 kg/m2
) in adulthood, accounting for a 39% increase in obesity after controlling for potential confounding variables38
. A recent prospective study examined the association between childhood sexual abuse and obesity among young adult females40
. Females with history of childhood sexual abuse were significantly more likely to be obese in young adulthood, however between-group differences were not significant during childhood or adolescence. The association between sexual abuse and OW/OB in the present sample may strengthen as the subjects are followed into young adulthood; however this remains to be determined. Nemeroff has hypothesized that significant early-life stress leads to greater stress responsiveness later in life, particularly via alterations in the corticotrophin-releasing factor (CRF) system41
. This system is involved, directly and indirectly, in multiple metabolic processes that could contribute to OW/OB, such as insulin resistance, inflammation, and autonomic regulation.
Aberrant regulation of consumptive behaviors may underlie both OW/OB and SUD, and this could account for the significant association between SUD and OW/OB in the present study. There may be shared functional neuroanatomical disturbances including reductions in striatal dopamine D2 receptors42
as well as altered serotonergic dynamics43
. However, recent findings from an epidemiologic study of adults with BP indicate that SUD and OW/OB may be inversely related7
. Further studies are needed to determine whether these discrepant findings are associated with developmental differences between youth and adults, differences between clinical and epidemiologic samples, or other factors as yet unknown.
Finally, the nature of the association between OW/OB and psychiatric hospitalizations merits further prospective investigation. This association could be explained by greater illness severity among OW/OB subjects precipitating hospitalizations. However the direction of this association is uncertain. Hospitalized youth are often exposed to highly caloric food options, have significant restrictions on physical activity and energy expenditure, and may be exposed to higher medication dosages. This study did not ascertain, and could not statistically examine, these factors.
Several limitations to the present study should be noted. First, this cross-sectional, observational study was not designed to examine medications in detail. Although categorical data were collected regarding current and lifetime exposure to a broad spectrum of medications, information regarding dosage, duration of treatment, and adherence was not ascertained at intake. Therefore, this study was not able to ascertain medication-related weight gain. Similarly, metabolic data were not collected. Since COBY is a prospective longitudinal study, in the future this sample will be able to provide more detailed data regarding medications and their propensity to cause weight-gain and OW/OB in this population. Second, as in several previous studies5,6,27
, height and weight (and therefore OW/OB) were indirectly ascertained. However, the reliability of self-reported height and weight in determining the OW/OB versus non-OW/OB dichotomy in a clinical sample at the Pittsburgh site was good-to-excellent. In addition, as detailed above, previous studies report that this method has good-to-excellent reliability, excellent specificity, and fair-good sensitivity23-27
. In the future, COBY subjects will all be measured directly such that future reports will not be constrained by this limitation. Third, the direction of the associations found in this study cannot be determined definitively. For example, it is unclear whether SUD preceded the development of OW/OB or whether the reverse is true, and the same applies for physical abuse, medication exposure, and psychiatric hospitalization. Fourth, data were not available regarding binge eating other than in the context of bulimia nervosa, or regarding exercise, nutrition, and metabolic indices. Such information could inform the understanding of the mechanism/s for OW/OB in BP. Similarly, data were not available regarding these youths’ dieting behaviors or perception of whether or not they were OW/OB, such that it remains to be determined how biases in weight perception among BP youth compare with those of non-BP youth and whether these biases are associated with dieting.44
Fifth, this study also did not consider the impact of family history of OW/OB or psychiatric disorders on OW/OB among probands. Finally, this study did not include healthy controls or psychiatric controls. Therefore, the high prevalence of OW/OB in the present study may not be specific to BP. Indeed, depressed mood has been associated with a two-fold increased incidence of obesity among adolescents45
, and depressive disorders and ODD may be more common among chronically obese youth46
. Future controlled studies are needed in order to directly compare the prevalence of OW/OB among youth with BP versus healthy controls and/or youth with other psychiatric conditions.